[Participate of nitric oxide participate in hypoxic regulation of cerebrovascular tension]

Sheng Li Xue Bao. 1996 Jun;48(3):222-6.
[Article in Chinese]

Abstract

Making use of nitric oxide synthesase (NOS) inhibitor Nw-nitric-oxide-L-arginine (L-NNA), the effect of NO and the pressence of endothelial cell on hypoxia-induced vascular dilatation was studied with new-born calve basilar artery. The experimental results show that L-NNA can attenuate the hypoxia-induced vascular dilatation, but the magnitude of attenuation is smaller than that of constriction caused by L-NNA on normoxic calve basilar artery. Under hypoxia, the vascular dilatation of endothelial cell denuded artery is smaller than that of endothelial cell intact artery; the difference between them is approximate by the same as the change caused by L-NNA on endothelial call intact artery. After destroying the endothelial cell, L-NNA has no obvious effect on the vascular tension. These results suggest that NO and endothelial cell are involved in hypoxia-induced vascular dilaxation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Basilar Artery / pathology
  • Basilar Artery / physiopathology*
  • Cattle
  • Endothelium, Vascular / physiology*
  • Hypoxia / metabolism
  • Hypoxia / physiopathology*
  • In Vitro Techniques
  • Nitric Oxide / physiology*
  • Nitric Oxide Synthase / antagonists & inhibitors
  • Nitroarginine / pharmacology
  • Vasodilation / physiology*

Substances

  • Nitroarginine
  • Nitric Oxide
  • Nitric Oxide Synthase